Guest Editor
Dr Ramnath Misra
Professor and head, clinical immunology
S.G.P.G.I.M.S, Lucknow

Dear All,

The association between myositis specific antibodies and acertain clinical subset/features of patients with inflmmatory myositis (IIM) led to the classification of patients based on the presence of autoantibodies. Whether this association applies to our country or not is important for the universal application of this classification. The recent publication (1) on the association between myositis-specific and associated autoantibodies (MSA and MAA) in patients andidiopathic inflammatory myositis (IIM) from North India revealed the prevalence and disease association for the first time and is a step forward in the applicability of this classification to India. Prior to this, there was only one study limited to 24 patients from our country that looked for MSA by using the gold-standard immunoblot assay, but the sample size was small enough to answer this question (2). A recently published study of 124 patients with IIM (DM-55, PM-25, JDM, and CTD-M – 22 each) is a fairly large cohort, as it is from a single centre. The sera were analysed by immunoblot and, in an ideal setting, should have been confirmed by the gold-standard immunoprecipitation assay. With the advent of commercial strips coated with recombinant or affinity-purified antigens, along with antibody conjugates, the test is widely available. The study in question employed the line blot assay. Ideally, the line blot assayfinding had to be confirmed the by immunoprecipitation assay.

Overall, the prevalence of both MSA (49%; anti Mi2–21%, synthetase consisting of Jo-1, PL-7,PL-12-23% and SRP [5%])and MAA was comparable to published reports from other countries [3], with some differences. Regarding MAA:antibodies to Ro (36%) Ku and PM-Scl (10%) and PM-Scl100 in 4%were found in three-fourths of IIM patients, while it is reported in more than 90% patients with IIM [3], since only immunoblotting was used whereas IB is combined with immunoprecipitation and ELISA and IB. The prevalence of anti-Mi-2 antibodies was higher in our cohort than reported from Europe [3]; this could be because of the higher number of patients with DM, which is itself associated with anti-Mi-2 antibodies. Anti-synthetase antibodies and antibodies to SRP in this report are comparable with published [4] reports. Fifty percent of the JDM sera were negative for all antibodies, probably because other antibodies (e.g. anti-p155/140 and anti-MJ) were not tested. Another contrasting observation was thepresence of anti-SRP antibodies more frequently in patients with DM as compared to patients with PM or CTD myositis.

This study validated the association between antisynthetase antibodies and ILD, mechanics hand and fever and polyarthritis (antisynthetase syndrome), and antibodies to Mi-2 in photosensitive skin rash in Indian patients with DM[3]. However, the complete absence of ILD in this subgroup of patients was an interesting finding, though the decreased prevalence of ILD in patients with anti-Mi2 antibody is known [5]. Similar to previous reports, most patients with anti-SRP antibody had refractory myositis with poor response to standard immunosuppressive therapies but showed improvement in muscle power with rituximab.

Regarding MAAs, as observed by others [3], anti-Ro52 was the most prevalent antibody distributed across all subtypes of IIM, with a lesser prevalence in the JDM group. Some interesting differences from previous reports are the association between anti-Ku antibodies in both adult and juvenile DM, and shawl sign distribution of anti-PM Scl antibodies in all categories of IIM rather than only with overlap connective tissue diseases and association of anti-Ro antibodies with antisynthetase syndrome. Anti Jo-1 antibodies are strongly associated with anti-Ro antibodies;therefore, this observation may not be due the latter. This study validates the earlier-described association between MSA and MAA and IIM. Some differences need to be substantiated in other parts of India. the study endorses the internal effort that clinical manifestations in IIM areinfluenced by the presence of aparticular set of autoantibodies that are specific and associated with the disease.

References

1. Shrivastava P, Dwivedi S and Misra R. Myositis specific and myositis – associated autoantibodies in Indian patients with Inflammatory myositis Rheum Int ; 36:935-943.
2. Chowdhary V, Aggarwal A, Misra R.Prevalence and Clinical Association of myositis specific autoantibodies in North Indian patients with idiopathic inflammatory myositis. APLAR Journal of Rheumatology 2000;4 (2):104-07.
3. Brouwer R, Hengstman GJ, Vree EW, Ehrfeld H, Bozic B, Ghirardello A et al. Autoantibody profiles in the sera of European patients with myositis. Ann Rheum Dis 2001;60:116–23.
4. Troyanov Y, Targoff IN, Tremblay JL Goulet JR, Raymond Y, Senécal JL. Novel classification of idiopathic inflammatory myopathies based on overlap syndrome features and autoantibodies: analysis of 100 French Canadian patients. Medicine(Baltimore) 2005;84:231-49.
5. Petri MH, Satoh M, Martin-Marquez BT, Vargas-Ramírez R, Jara LJ, Saavedra MA, et al. Implications in the anti-Mi2 and the anti-p155/140 autoantibody prevalence in two dermatomyositis cohorts from Mexico City and Guadalajara. Arthritis Res Ther. 2013;15:R48.